The spread of cancer generally consists of numerous genetic and epigenetic factors that result in uncontrolled cellular proliferation, invasion, increased cell survival and metastatic spread. Current methods for treating cancer have limitations. For instance, though systemic chemotherapy remains palliative, it is only modestly effective. Furthermore, due to its non-specific nature, systemic chemotherapy results in numerous undesired side effects. Accordingly, targeted therapies, including inhibition of receptor tyrosine kinases, are more desirable for treating cancer. Many such therapies, such as growth factor inhibition, use algorithms that take into account target expression and validation of molecular pathways. For instance, growth factor receptors, such as the epidermal growth factor receptor (EGFR), fibroblast growth factor receptor (FGFR), or platelet-derived growth factor receptor (PDGFR) are differentially expressed by bladder cancer cell lines or tumors, making inhibitors to these molecules attractive therapeutic tools. In fact, inhibitors of the epidermal growth factor receptor (EGFR) are being evaluated for use in the treatment of urothelial cancers and other solid malignancies.
However, many cancer cell lines remain resistant to targeted therapies. For instance, many bladder cancer cell lines remain resistant to EGFR-directed therapy. Furthermore, it is at times difficult to assess or predict the resistance of cancer cell lines to targeted therapies due to the absence of ascertainable biomarkers.
Accordingly, there is currently a need to enhance the sensitivity of cancer cells to targeted therapies, such as EGFR-directed therapy (anti-EGFR treatment). There is also a need to identify biomarkers that can be used to assess the sensitivity of cancer cell lines to targeted therapies.